Effect of amyloid β-protein on chemokine (C-C motif) ligand 5 expression and nuclear transcription factor κB signal pathways

Abstract

Objective To explore the effect of amyloid β-protein (Aβ) on chemokine (C-C motif) ligand 5 (CCL-5) expression and nuclear transcription factor κB (NF-κB) signaling pathways. Methods The tumor model of mouse oral cancer was constructed by using Aβ-Tg transgenic mice and C57 mice, and the role of Aβ on oral cancer growth was studied.Using protein chip technology, the protein witch was differential expression in Aβ-Tg transgenic mice and C57 mice serum were selected, and the expression of this protein was determined by ELISA and immunohistochemistry.The effect of Aβ on the CCL-5 expression and NF-κB signaling pathway were studied by immunoprotein imprinting technique. Results Compared with C57 mice, the Aβ-Tg transgenic mice was significantly reduced in the oral cancer volume and weight, and the survival period was significantly prolonged (P<0.05). Protein chip technology screening results showed that Aβ was applied to the CCL-5 of oral cancer.Furthermore, the expression of CCL-5 mRNA level of Aβ-Tg transgenic mice was significantly lower than that in C57 mice (P<0.05). The results of ELISA test results CCL-5 protein level was significantly lower than the control group (P<0.05). The results of immunoprotein imprinting of tumor tissue protein tumor in oral cancer model showed that P50, P65 phosphorylation and tumor necrosis factor-α expression in Aβ-Tg transgenic mice were significantly lower than that of C57 mice(P<0.05). Conclusion Aβ activated the NF-κB signaling pathway by reducing the secretion of CCL-5 by macrophages and inhibited the growth of oral cancer of mice. Key words: Amyloid β-protein; Chemokine (C-C motif) ligand 5; Oral cancer; Nuclear transcription factor κB